Evidence map›Paper›PMID 35833296›Full record

ArticleHaematologica2023

PDL1 shapes the classical Hodgkin lymphoma microenvironment without inducing T-cell exhaustion.

Joseph G Taylor, Edward Truelove, Andrew Clear, Maria Calaminici, John G Gribben

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Joseph G TaylorCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ; Barts NHS Trust, St Bartholomew's Hospital, West Smithfield, London.
Edward TrueloveCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ; Barts NHS Trust, St Bartholomew's Hospital, West Smithfield, London.
Andrew ClearCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ.
Maria CalaminiciCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ; Barts NHS Trust, St Bartholomew's Hospital, West Smithfield, London.
John G GribbenCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ; Barts NHS Trust, St Bartholomew's Hospital, West Smithfield, London. j.gribben@qmul.ac.uk.
St Bartholomew's Hospital · GBQueen Mary University of London · GB

Funding

Wellcome TrustWellcome Trust 200144/Z/15/Z
6 · The paper itself

Abstract

Classical Hodgkin lymphoma (CHL) is unusually sensitive to PD1 inhibition and PDL1 is highly expressed on CHL cells and in the tumor microenvironment. This could be interpreted as evidence of exhaustion, but paradoxically, PD1+ lymphocyte infiltration does not predict response to PD1 inhibitors and no increase in cytotoxic markers is seen after PD1 therapy as might be expected with reversal of exhaustion. In contrast to PD1, elevated PDL1 does predict response to PD1 inhibitors and recent data associate both retained CHL MHC-II expression and increased T helper (TH) T-cell receptor diversity with response, suggesting a connection to the TH compartment. We performed a phenotypic, spatial and functional assessment of T-cell exhaustion in CHL and found co-expression of an exhaustion marker and lower PD1 expression in CHL than in reactive nodes whereas the proliferative and cytokine production capacity were similar in CHL and the reactive nodes. We found no correlation between PDL1 expression and exhaustion signatures. Instead, we identified a strong association between PDL1 expression and CHL MHC-II expression, TH recruitment, and enrichment of TH1 regulatory cells. These data suggest that a dominant effect of PDL1 expression in CHL may be TH engagement and promotion of a regulatory microenvironment rather than maintenance of exhaustion.

Indexed as

Hodgkin DiseaseB7-H1 AntigenHumansProgrammed Cell Death 1 ReceptorT-Cell ExhaustionTh1 CellsT-Lymphocytes, Helper-InducerTumor MicroenvironmentB7-H1 AntigenPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID35833296
PMCPMC10071123
OpenAlexW4285386927

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.